The Effects of Diet On Testosterone Parts 1 & 2

The Effects of Diet on Testosterone Part 1: Calories and Proteinby Thomas Incledon and Lori Gross

Introduction
This article will be divided into two parts. Part 1 presents an overview of how testosterone is stimulated in the body, shows how calorie balance affects T production, and discusses how dietary protein intake affects circulating T levels. Part 2 explains how carbohydrates and fats impact testosterone synthesis and circulation, and then puts it all together for you to make informed decisions. Keep in mind that this is a very complicated and dynamic process. References will be limited primarily to studies on men. However, animal research will be cited when it becomes necessary to discuss proposed mechanisms, or how the actual changes in the body take place. While the information may get technical at times, read on because you will learn a great deal that you may wish to apply to your own diet.

The HPT Axis
An article on the effects of diet on hormones would be incomplete without a basic overview of the relationships between the organs and hormones of the axis. The term axis simply refers to the pathway in question. The glands of this pathway include the hypothalamus, pituitary, and testes. The sequence of events culminating with the production and/or release of T begins at the hypothalamus. Here specialized nerve cells release a hormone called gonadotropin-releasing hormone (GnRH). GnRH is a decapeptide (chain of ten amino acids) that travels by direct blood vessel connections to the anterior pituitary where it stimulates the release of luteinizing hormone (LH) (1). LH is then secreted into the blood where it attaches to receptors on the Leydig cells of the testes. This induces activity of an enzyme, P-450scc, referred to as the cholesterol-side-chain-cleavage enzyme (1). Through a series of five enzymatic steps, cholesterol is converted into T.

The body regulates the circulating blood levels of T via several mechanisms. Once in the blood, about 44% of T is bound to a protein called either sex-hormone-binding-globulin (SHBG) or testosterone-binding globulin (TeBG), to indicate the greater affinity for T over estradiol (E2, an estrogen). About 54% of T is bound by albumin and other proteins, leaving 2% to circulate unbound to any protein. This unbound T is termed free testosterone (fT) (1). It is currently believed that only the fT or albumin bound T are truly available to interact with the tissues of the body. The significance of this point will be elaborated upon later in reviews of the data from different studies. Of the T that is available to interact with tissues, some of it binds to steroid receptors. In most tissues, like skeletal muscle, it will directly stimulate protein synthesis. In some tissues, like the brain and fat cells, it can be converted into E2 via the aromatase enzyme. In other tissues, like the prostate gland, it can be converted into dihydrotestosterone (DHT) via the 5-alpha-reductase enzyme. T either directly or through conversion to E2 or DHT can inhibit its own future production. The conversion to E2 or DHT can take place both in the brain and various other tissues. E2 and T exert stronger inhibitory effects than DHT on T production. This process is called negative-feedback inhibition. This is the reason why the use of steroids, enzyme inhibitors, and prohormones are far from perfect in their effects on increasing T levels. Because it is a dynamic process, as T levels elevate in the blood, a corresponding increase in inhibitory signals occurs. This results in the body making less T. The opposite occurs when T levels decrease. This is a basic overview and presented in a simplistic static fashion. The body is a highly dynamic organism and many factors come into play to help regulate this process. This point is made to illustrate the confounding problem that occurs when trying to increase circulating levels of androgens.

Effects of Calorie Intake on Testosterone
Every minute of the day, someone makes a decision to lose weight. Dieting by means of restricting calories, while not always successful, is practiced frequently. There are some people who believe that fasting (or what we call planned starvation) is a necessary method for cleaning the body of wastes. What effects does depriving the body of calories have on endocrine responses within the HPT axis? As you may have already guessed, it screws things up. Fasting for 5 days can lower LH, T, and fT by 30-50% (2). What appears to happen is that as the body becomes deprived of energy, less GnRH is released from the hypothalamus. This, in turn, leads to a weaker signal to release LH. While the pattern of LH release remains the same, the amount of LH released at each interval decreases, meaning your body is giving weaker signals to stimulate T. In addition, research on fasting in rats indicates that testicular enzymes involved in synthesizing T decrease in function (3). This means that even if enough LH reaches the testes, they still cannot produce normal amounts of T. The decrease in T can be a contributing factor to the loss in lean body mass that occurs with fasting. Of course, this is contrary to what most of us want to do in the quest to get bigger and stronger. However, many elite athletes have learned how to apply fasting to their contest preparation. Fasting before a drug test is a common practice when on anabolic-androgenic steroids because it helps prevent testing positive. But before you run out and load up on some "juice" and think you’ll beat a drug test just by fasting, keep in mind that this method is not always reliable, nor does it work when you have foreign metabolites in the body.

One of the common problems when dieting is holding onto all that hard earned muscle. Severe calorie restriction, whether from reduced food intake or imposed by excessive exercise, lowers testosterone (4). While there are no numbers written in stone, a decrease in calories by 15% does not lower T levels (5). This may serve as one factor to consider when planning out a diet strategy. If you cut back too much on your calories, then you risk lowering your T, which can cause you to say goodbye to some of your muscle. The good news is that when refeeding resumes and calorie intake equals calorie expenditure, in most cases, T levels will rise back to normal. The bad news is that if you are engaging in chronic high volume endurance exercise, even extra calories won’t help raise your T levels back to normal.

When male subjects are overfed in an attempt to induce weight gain, there tends to be a decrease in T levels as upper body fat increases (6). It may be wise, therefore, to limit calorie intakes to less than 1000 Calories (kilocalories) above energy requirements. From reviewing the literature, it seems that with large short-term increases in body fat and small chronic increases, T levels go down. Perhaps this is due to an inverse relationship between T and insulin and/or the aromatase enzyme. It is clear that with excessive body fat, aromatase activity in fat cells increases, thus more of T is converted into an estrogen called estradiol (E2). The issue with insulin is far more complicated and not really clear. Some research has shown insulin to regulate T in a positive fashion (7), while carbohydrate and protein liquid meals, which elevate insulin, have been shown to decrease T in resistance- trained males (8,9). This may be due to an increased uptake by tissues, like skeletal muscle, increased excretion of T in the urine, or decreased responsiveness of the testes to produce T.

While not related to caloric intake, hydration and sleep status are also important. A reduction of 3.8% in body weight due to dehydration did not affect T levels during mild exercise (10). But, don’t take any chances with hydration. Drink plenty of water every day at the rate of 30 cc per kilogram of body weight (or roughly one ounce for every two pounds). Get plenty of sleep, as disturbances in sleep and light/dark cycles can decrease T by almost 50% (11). Of course, no one ever gets enough sleep!

Dietary Protein Intake & Testosterone
The direct impact of protein by itself on T levels has not been well studied in humans. Some research on high protein diets deals with the effects on very obese people and weight loss. While this may not seem applicable to you, read on and we will put it together for you. In obese men, feeding 600 calories a day with 400 calories from protein (50 grams of beef protein and 50 grams of casein) induces lower levels of T than fasting does (12). Normally, when the kidneys filter T out of the blood, some T gets reabsorbed back out of the kidneys into the blood. The researchers stated that the additional protein in the diet generated more ketones. They concluded that the ketones were filtered out of the blood by the kidneys and were reabsorbed back into circulation preferentially over T. While most people reading this may not be obese, higher protein diets are definitely in vogue, more so for bodybuilders and powerlifters than other groups of athletes. The potential exists that if a ketogenic diet like the Atkins Diet or a cyclical ketogenic diet like the Anabolic Diet or Bodyopus is followed, than urinary excretion of T will be greater during the ketogenic phase of the diet.

It is known that protein in the diet can influence the metabolism of a variety of chemicals. Through a series of experiments, it was demonstrated that various foods could influence the metabolism of drugs in the body (13). Vegetables like cabbage and brussel sprouts were found to alter the function of specific liver enzymes. This, in turn, could change the half-life of a drug in the blood. Given the variety of diets that people follow and the variety of prescription medications and over-the-counter drugs people take, the logical progression was to look at how altering the macronutrient composition of the diet affected drug metabolism. It turns out that a higher ratio protein diet, a diet with more calories from protein than carbohydrates or fat, metabolizes some drugs faster, thus decreasing the clearance time of the drug. Since diet can affect drug metabolism, perhaps it could affect liver enzymes involved in the metabolism of endogenous steroids. Sure enough, it was found that a high ratio protein diet decreased the reduction of T (14). Reducing the reduction of T could mean a potential decrease in DHT and/or androsterone in the blood, which is good by most accounts. However, DHT levels were not measured and, more importantly, urinary T excretion increased, although it was not statistically significant. These subjects were not in ketosis, so perhaps ketones do not increase T excretion rates. Regardless of the exact mechanism, there is sufficient evidence in the literature that when protein intake exceeds carbohydrate intake, T clearance increases by excretion in the urine.

A cross over design study used seven normal men from 23-43 years of age and compared a high protein diet to a high carbohydrate diet (15). This study has been referenced many times and cited as proof that high protein diets lower total T levels in the blood. The high carbohydrate diet from this study will be covered in Part II. The high protein diet consisted of 44% protein, 35% carbohydrate, and 21% fat and supplied between 2400 and 2500 kilocalories per day (kcals/d). Let’s assume it was an even 2450 kcals/d. The men also had bodyweights that ranged from 64-72 kg. If we assume the mean was 68 kg, then this would give us an average body weight of about 150 pounds. This means these guys were eating [(2450 kcals/d times .44) (divide by 4)] 270 grams (g) of protein, [(2450 x.350 /4] 215 g of carbohydrates (CHO) and [(2450 x .21) /9] 58 g of fat per day.

However, total T is not that big of a deal. The more important measure is the bioactive fraction of T. (Earlier in the overview of the HPT Axis, it was mentioned that SHBG-bound T is not considered bioactive, while the other fractions of T are). While subjects followed the high protein diet, their total T levels were 28% lower than on the higher CHO diet (15). This is important because T decreased in all seven subjects, although the magnitudes of the decrease ranged from 10 to 93%. For the same seven subjects, their SHBG levels decreased about 39% with a range from 19 to 64%. Looking at this data gives the impression that the actual bioactivity of T was higher while the subjects were on a high protein diet. SHBG-bound T and fT were not measured, so it is not known for sure. On the surface it appears that a mean decrease of 39% in the SHBG values and only a 28% in the T would leave more T available for binding to tissues. However, if we calculate out the actual changes in the hormones using the data from the study, we see something different. The mean and standard error (M±SE) for T was 371 ± 23 ng/dL. The currently used units in clinical chemistry are nmol/L. Multiplying the mean T by the conversion factor of 0.0347 gives us about 12.9 ± .8 nmol/L. The M±SE SHBG was 23.4 ± 1.6 nmol/L. If we assume that the amount of T bound to SHBG averages 44%, then .44 x 12.9 ± .8 nmol/L gives us 5.7 ± .4 nmol/L of T bound to SHBG. That leaves 7.2 ± .4 nmol/L of T to interact with tissues in the body. However, we don’t know from the data if the amount of SHBG bound T decreased below or increased above the normal 44%, in which case there would be more or less T available to interact with tissues.

From work by the same group of researchers using the exact same diet (but different subjects) we see that the ratio of 5a - reduction to 5b - reduction (5a /5b ) of T is reduced by about 50%, with the decrease being attributed to lower rates of 5a - reduction (14). The T values that have been used thus far (15) already reflect any changes in altered T metabolism, so the conversion to a 5a - reduced hormone (ie androsterone) is accounted for at this point. Note that even though there is a decrease in 5a - reduced hormone production, it does not show up as increased T levels. The decrease in androsterone probably shows up in small, but statistically insignificant increases in other metabolites of T (they were statistically insignificant perhaps due to the small sample size). Another interesting aspect is that there is an increase in the oxidation of estradiol on the higher protein diet by about 14-15% (14). Unfortunately estradiol levels were not measured in this paper. This could have given us clues as to the mechanism by which higher protein diets lower T (ie increased negative feedback on T levels via estradiol). At this point, this is only one study and it is still difficult to come to any final conclusions. However, if this is what really happens, then a high-protein diet may actually lower the anabolic actions of T in the body. Unfortunately, this has not been verified through laboratory research and is just a theory at this point. Perhaps the decrease in T is a result of increased excretion in the urine either as T or a sulfated metabolite, or increased conversion to estradiol and oxidation by the liver.

Prelude to the Effects of Diet on Testosterone Part II: Carbohydrates and Fat
We hope so far that you have learned something about testosterone production and the effects of calorie intake and protein intake on testosterone levels in the blood. Please feel free to contact us if you have any questions or comments at lorig8r@sprynet.com . In the next article, the effects of carbohydrates and fat and total T levels and its components are explained. We will then review the key points and see how the information can be integrated into a diet strategy. At this point we would like to thank Albert Jenab for his technical assistance and insight.

14) Kappas A. Anderson KE. Conney AH. Pantuck EJ. Fishman J. Bradlow HL. Nutrition-endocrine interactions: induction of reciprocal changes in the delta 4-5 alpha-reduction of testosterone and the cytochrome P-450-dependent oxidation of estradiol by dietary macronutrients in man. Proceedings of the National Academy of Sciences of the United States of America. 80(24):7646-9, 1983 Dec.

The Effects of Diet on Testosterone (Part 2): Carbohydrates and Fatsby Thomas Incledon and Lori Gross

Introduction
Part One of this article explained the impact of calories and dietary protein (PRO) on endogenous testosterone (T) levels. As promised, this continuation will focus on the role of dietary carbohydrates (CHO) and dietary fat on modulating T production. The role of CHO on T production is indirectly addressed when discussing the role of PRO or fat, so this will be reviewed briefly. The effects of fat on T are far more complicated and often time more confusing than the previously discussed macronutrients. To facilitate an understanding of the links between dietary fats or lipids and T, several tables will be presented. An explanation will accompany each table and key references will be reviewed. The article ends with an application of the information to the design of a dietary strategy to either maximize or minimize T levels.

Dietary Carbohydrate Intake & Testosterone
Dietary carbohydrates can influence the metabolism of a variety of chemicals. When fat is held at approximately 20% of caloric intake, CHO may elevate T levels (1). Part One of this article discussed that while this may be true, there is also a corresponding increase in sex hormone binding-globulin (SHBG). Anderson et al (1) compared the effects of a higher PRO diet versus a higher CHO diet on T levels. Part one discussed the data on the high protein diet. The higher CHO diet contained approximately 2450 kcals/d, 70% CHO, 10% PRO, 20% fat. This provides 429 g/d CHO, 62 g/d PRO, and 55 g/d fat. The seven men in this study had a range of body weights from 64-72 kg. If a mean of 68 kg is assumed, then these subjects were taking in .91g PRO/kg BW or slightly higher than the RDA of .8g/kg BW. This point is made because most people take in more protein than this on a daily basis.

Now let’s get back to the T and SHBG issue. The interaction between T and SHBG is important to consider. About 44% of total T is bound to SHBG and is called SHBG-T. If T increases more than the SHBG-T fraction does, then the biological actions of T will be greater because more of it will be available to bind to muscle and other tissues’ receptors. If T increases less than SHBG-T fraction, then the biological actions of T will decrease because less of it will be available to bind to muscle and other tissues’ receptors. Anderson et al did not measure SHBG-T. The study did measure total T and SHBG. It can be seen from their data, that T increases less than SHBG did on the higher CHO diet with a ratio of 7:1 (CHO:PRO). The T values were 16.2 ± 1.2 nmol/L. This was a 28% increase over the high PRO diet and the range of increases in the subjects was from 10-93%. Assuming that the SHBG-T fraction remained at 44% of T, then the amount of T that was bioavailable would be about 9.1 ± .66 nmol/L. Compared to the amount of bioavailable T on the high PRO diet, there is an additional 1.9 ± .21 nmol/L of bioavailable T.

Also keep in mind that this same type of diet increases the ability of the liver to reduce T to 5a - reduced hormones (ie androsterone) (2), which may or may not be something you want (depending on the study you read). However, this is especially important for steroid and prohormone users because a higher CHO diet may increase the conversion of the exogenous T to androsterone. This is not to say that diets with higher CHO than PRO will cause this to occur. What this means is that very high CHO:PRO ratios like 7:1 or greater may not be the healthiest way to go, based upon direct and indirect evidence that androsterone is linked to acne and prostate disorders.

The effects of CHO on T were just discussed while fat was kept constant in the diet at about 20% of calories. When PRO is kept constant in the diet, higher CHO may actually lower T (8). Hamalainen et al (8) compared the effects of a dietary intervention on the hormone levels of 30 men. PRO intake was fairly consistent while the CHO was increased from 45% to 56% of calories for six weeks, and then decreased to 47% for six weeks. Fat intake was correspondingly decreased from 40% to 25%, and then increased to 37%. During the higher CHO period, T and fT decreased significantly. However, this study was difficult to interpret because dietary fibers, like pectin from fruit or bran from wheat, and fatty acids, like saturated fatty acids or polyunsaturated fatty acids, can also have an impact on T production. In the Hamalainen et al study, they also changed the fatty acid ratios of the diets. Perhaps the ratio of fatty acids, as opposed to the amount of CHO or fat, had a larger impact on T production. Extrapolating this further, maybe it is not the amount of CHO or the CHO:PRO that influences T production, but the ratio of CHO to a particular fatty acid, or some other nutrient interaction (ie PRO to fatty acid or ratio of fatty acids).

Correlation Studies Between Dietary Fat Intake and Testosterone Levels in Men
Fat has received tremendous attention over the last few years and has been linked to improved performance and favorable body composition alterations in the lay journals, despite a lack of convincing scientific data. The relationship between dietary lipids and T is important in order to understand the role that fat may have in improving performance, altering body fat, or preventing/initiating disease.

One of the reasons why the scientific data has not been clear in explaining the role of dietary fat on T levels is a difference in study designs. Table 1 displays the data and results from several studies that compared T, free testosterone (fT), and/or SHBG levels with total fat or types of fatty acids in the diet. Data is listed as the mean values (when available). Correlation studies, while very common, are far from complete. They don’t explain if dietary fat or some fraction, like polyunsaturated fatty acids (PUFA), affects T, rather they only state if there is a relationship between one event and another. The relationship can be positive and an example of this is reference 19 from Table 1. From the results column the code FCT is listed in the results column. FCT means that as the percentage of calories from fat, grams of saturated fat, and grams of monounsaturated fat (MUFA) increased in the diet, there was also a corresponding association with higher T levels. This study was done with resistance trained males and is the most applicable from all of the above studies. The scope of this article precludes an in-depth analysis of each study and the associated design flaws. Most important is to cite the common findings. From Table 1, several relationships can be seen. Subjects consuming vegetarian diets have demonstrated higher SHBG levels (3, 13), lower T levels (12), and lower levels of available T (3). One flaw with many of these studies is isolating the impact of fat on the diet as opposed to fiber, which is also much higher in vegetarian-type diets. Another problem with correlational studies is that they don’t tell you what happens when subjects are switched from one type of diet to another. Unfortunately studies sometimes contradict each other. For example, Bishop et al (4) examined the role of dietary nutrients on sex hormone differences between monozygotic twins (identical twins). The investigators found an inverse (or negative) relationship between dietary fats and T. Volek et al (17) however, found a positive relationship between dietary fat and T. This further demonstrates the problem of reading the scientific literature and making sense of all the information.

Acute Effects of Dietary Fat on Testosterone
A better study design than a correlational study to determine the effects of manipulating dietary macronutrients is a randomized cross over, double-blind study. Cross over means that every subject experiences all of the different dietary treatments. By randomizing the order, the effect of one diet on another is avoided (this is called order effect). Double-blind means that the subjects, the people working with the subjects, and the people tracking the data are all unaware of the treatment conditions. This is very difficult to do with feeding studies, so in most cases a double-blind approach is not used. Therefore, in most studies, the subjects and/or the researchers know what the treatment conditions are. One way the researchers avoid this problem is to offer milk shakes that taste the same, but, in fact, have different macronutrient compositions. While this may be acceptable to study the acute effects of more or less fat in a meal, this would not work for chronic studies. After all, could you drink the same milkshake all day long for weeks and weeks, or worse yet eat some type of engineered food product not knowing what was inside?

Acute studies examine the effects of different treatments within the hours or days after the dietary manipulation. In general, the subjects are given different types of diets and the results of each diet are compared. This is one way to look at the effects of a particular nutrient on hormone levels or blood glucose levels, for example. Table 2 presents the tabulated data from two short term or acute studies.

In one study (14), the effects of high fat (HF) and low fat (LF) meals on T levels were compared. The subjects were given a lemon-lime artificially sweetened beverage and the hormonal responses served as a control (C) for the other meals. A HF liquid meal containing about 795 calories and made up of 57% fat (50.4 g fat), 9% protein (17.9 g PRO), and 34% carbohydrate (67.5 g CHO) was given on another occasion. The third or final liquid meal (LF) consisted of 797 calories made up of 1.2% fat (1 g fat), 25.5 % PRO (51 g PRO), and 73.3% CHO (146 g of CHO). The C and LF meals did not effect luteinizing hormone (LH), T, fT or dihydrotestosterone (DHT) levels. The HF meal decreased T and fT up to 4 hours post ingestion compared to the other liquid meals without affecting any of the other hormones.

There are some problems with this study, however. It was not double-blind, the treatments were not randomized, it used a small sample size of eight, and while the subjects were instructed to fast, no data was offered to confirm this, like blood sugar levels. The study also did not look at the possible mechanisms by which the HF diet lowered T and fT levels.

It has been proposed in the literature that fatty acids may bind SHBG. If this is true, then after the fat is broken down from a high fat meal, a corresponding increase in blood fatty acid levels would occur, and less SHBG is available to bind with T. This would then increase the percentage of fT in the blood. However, since the percentage of fT in this study did not change (the total amount decreased, not the percentage of total T), this could not have occurred. The researchers do offer that the only way that the HF meal could have affected T/fT levels was either by increasing the clearance rate or decreasing the production rate. The clearance rate would be determined by the rate of uptake by tissues, the rate of T and fT metabolized by the liver, and the rate of excretion by the kidneys. While fatty acids do attach to T and fT inside the body, there is no data to say that this increases uptake into tissues like skeletal muscle or that the event could occur within four hours post-meal ingestion. It would be unlikely that the fatty acids from the meal could affect the liver enzymes involved in T or its fractions so soon. It is possible that ketones produced from the breakdown of the fatty acids could cause the renal tubules to excrete more T and fT. But this is unlikely due to the fact that the subjects were not in a glycogen-depleted state and there were PROs and CHOs in the meal. This leaves decreased production of T and fT as the most likely reason for the drop in these hormones. Again, this is only speculation at this point since the study did not examine the possible causes for the decrease in the hormones.

Chronic Effects of Dietary Fat on Testosterone
The chronic studies presented in Table 3 report the effects of 2 or more weeks of dietary manipulations on testosterone levels. A decrease in dietary fat has been shown to decrease total T (8, 11, 15) and fT levels (8, 16) or not affect T levels (17). Approaching this from the other direction, an increase in dietary fat has been shown to decrease total T (11), and increase (16) or decrease fT levels (6). It’s not necessary to review all the studies to try to explain the differences in results. However, notice that from the Table 3, most studies compared vegetarian-type diets to western-type diets. This presents several problems when trying to explain the hormonal responses from the dietary manipulations. The first is that other dietary factors were altered in addition to fat intake. These included fiber content and the presence of various phytonutrients like flavonoids, isothiocyanates, etc. The main point is that there are many factors that can determine the effects of dietary fat on T levels. Most studies did not even report the amounts of fatty acids in the subjects’ diets, let alone the content of phytonutrients, so these factors were most likely not controlled for. Furthermore, differences in the length of the treatments (2 weeks vs. 10 weeks), lifestyles of the subjects (active vs. sedentary), and calorie loads (2800 vs. 4374) are additional examples of factors that can impact the results.

All the Evidence Not In Yet
It has been speculated that the ratio of fatty acids may have some role on whether or not dietary fat increases or decreases T levels. A positive relationship between saturated fatty acids and monounsaturated fatty acids with T levels has been reported previously (19). The same data also describes a negative (or inverse) relationship between polyunsaturated fatty acids and T levels. These relationships between dietary fat components and T have also been supported by a study on eight men randomly assigned and crossed over from a vegetarian diet to a mixed-meat diet that was isoenergetic (15). About 28% of the calories were from fat. The vegetarian diet had a polyunsaturated fatty acid to saturated fatty acid ratio (P:S) > 1, while the mixed-meat diet had P:S of about .5.

In a 1996 study, forty-three men were exposed to a high-fat, low-fiber diet for 10 weeks and a low-fat, high-fiber diet for 10 weeks in a cross over design (6). Total T and fT did not change significantly. SHBG-bound T was higher on the high-fat diet, which does not agree with another study (16). The researchers claimed this might have been due to within-person variations of plasma testosterone levels.

Another important finding was that urinary excretion of T was much greater on the high-fat, low-fiber diet (6). Other studies have shown that on higher fat diets, urinary excretion of T is increased (10, 11) while vegetarian type diets may decrease the urinary excretion of T (9, 10, 11). This is an important point to consider in evaluating the level of T bioactivity in the body. If blood levels of T elevate and the excretion rate of T also elevates there may not be a net bioactive effect of T. However, if blood levels of T remain the same and T excretion decreases, that may signal a net bioactive effect of T in the body. While it is difficult to say if a higher fat or lower fat diet would be better for increasing the bioactivity of T, it does appear that higher fat and lower fiber-type diets are associated with greater excretion of T. An increase in the urinary excretion of T combined with an elevation of T levels in the blood may indicate that the net T production is greater. The implication is that cells may have an increased opportunity to be exposed to T. Alternatively, perhaps it is the result of some type of self-regulating mechanism that the body maintains to keep endogenous levels in check.

There are many more studies in the literature. The intent was to expose the reader to all the different possible interactions and the complexity in trying to control for all areas just to determine the role of fat on androgen production. Other studies have examined the effects of different fatty acids on testicular cell membranes and T levels after supplementation fatty acid supplementation. The results do not support one another and only point to the fact that dietary fat plays a role in modifying T production, but that role is still unclear.

Designing A Diet to Maximize Testosterone Levels
Remember, it is the bioactive fraction of total T that is important. This fraction consists of fT and albumin-bound T. Fasting suppresses T production and small amounts of either PRO or CHO do not reverse the suppression. Diets with a PRO intake greater than the CHO intake lower total T levels, and may actually decrease the bioactivity of T in the body. Higher CHO diets (70% or more from CHOs) may increase T levels, but they also affect the metabolism of T as well. While the role of fat is not entirely clear, saturated fat and cholesterol are closely linked to higher levels of T and PUFAs have some modifying role.

So, what is the best type of diet to follow if your only concern is to increase T levels and make more of it available to the body for the purpose of improving lean body mass and/or performance? It would seem that CHO intake must exceed PRO intake by at least 40% to keep the bioactive fraction of T high. Fat intake should be at least 30%, saturated fat needs to be higher than PUFA, and fiber intake needs to be low. A sample diet would have roughly the following calorie breakdown: 55% CHO, 15% PRO and 30% fat. On the other hand, what if you wanted to lower your T levels in order to minimize cardiovascular disease risk factors and/or hormone-dependent cancer risks? Then a diet with more protein, more fiber, a fat intake below 25%, and a P:S ratio of 1 or higher would be a more prudent choice. The breakdown of this sample diet would be about 50% CHO, 30% PRO and 20% fat. The problem with using percentages, however, is that people with high calorie needs will most likely take in far more protein then they need. Another strategy is to keep protein intake the same (ie 1 gram per pound of BW) and then play around with the fiber, SFA:PUFA ratio, CHO, and total fat contents of the diet. Antioxidants are important additions when trying the higher fat diets. Keep in mind there are many factors that affect T production and they interact in a complex and seemingly unpredictable fashion. We invite feedback and will respond to all questions, comments, etc. Several readers have mentioned the idea of cycling a diet that maximizes T and then switching back to a healthier type of diet. For those that do try this, please let us know your results. lorig8r@sprynet.com.

Kappas A. Anderson KE. Conney AH. Pantuck EJ. Fishman J. Bradlow HL. Nutrition-endocrine interactions: induction of reciprocal changes in the delta 4-5 alpha-reduction of testosterone and the cytochrome P-450-dependent oxidation of estradiol by dietary macronutrients in man. Proceedings of the National Academy of Sciences of the United States of America. 80(24):7646-9, 1983 Dec.